XMRV infection rate points to cofactor not sole cause

I read a few articles on the XMRV studies and they stated researchers felt that XMRV was a trigger and/or coinfection but not the sole cause. I did some basic math and think I figured out why. This is very encouraging because it means that exposure isn't anymore than a temporary illness unless you have the cofactor present. I believe the cofactor is L-form, cell wall deficient bacteria. Logically you can cure the disease by killing the bacteria.

The incidence of chronic fatigue syndrome in the USA is 0.7% of the population. (2.2 million patients/307 million total population).

The reported healthy control group rate for XMRV incidence was 4%.

Therefore the XMRV incidence was lower in control non-CFS patients than the incidence in the general population. We expect it to decrease if XMRV is triggering it and the percentage tells us whether or not cofactors are involved. If CFS is only caused by XMRV there should be a 100% decrease with none not getting infected. According to this data, CFS incidence increased by only about 75%, but not 100%. So 25% [calculated as(7%-4%)/4%] of those infected don't get CFS from XMRV infection, the rest are infected. Why? There must be a cofactor...hence L-form bacteria and other conditions (vitamin D intake, sun exposure, etc).

Correction: due to a math error previous XMRV rate was overestimated. Using the new figure, this provides compelling evidence that XMRV is just a trigger.

The problem with this argument is that it assumes that (a) CFS is a well-defined single condition, and (b) the detection of XMRV by those researchers who are finding it is 100% accurate with no false negatives.

Since "CFS" is clearly not well-defined, and there are almost certainly going to be misdiagnoses in the population diagnosed "CFS", any arguments based on such percentages are based on a false assumption. It just isn't useful to make those sort of arguments about percentages found in CFS studies based on the assumption that "CFS" is a single entity. That kind of spurious argument has been used greatly to suppress research into ME/CFS. It's such disingenuous behaviour it's hard to credit that it isn't done deliberately, and yet when one talks to doctors and supposedly intelligence people about CFS, one discovers that people really are that stupid.

More importantly in this case, though, is the fact that XMRV detection is in its infancy. To achieve 75% detection rates is extraordinary enough at this stage of understanding; there's no reason to believe this figure won't increase. Indeed an as-yet-unpublished paper by the WPI is said to find 95% infection rate in the patients they studied, probably reflecting their expertise in distinguishing "true" (XMRV) ME/CFS as much as anything else.

More importantly still, XMRV is believed to be a "stealth" retrovirus, lying dormant in infected tissue until triggered by factors like levels of stress, hormones and inflammation. So XMRV can easily be lying dormant in individuals that test negative, and the controls who test negative could well develop ME/CFS in the future.

Having said all that, I think one thing we can say is that based on the early data, it would appear that only roughly 10% of those infected with XMRV are currently diagnosed with ME/CFS (assuming 7% general population with XMRV infection and 0.7% with ME/CFS). So this does indeed suggest to me that - as the WPI and Dr Coffin have said since day one - there very probably are co-factors influencing ME/CFS development, and as just one simple example, it could be that only about 10% of the population have the relevant (innate or acquired) deficiencies in RNAsel or APOBEC3 pathways which mean they are unable to 'reprogram' XMRV infection.

So in summary: yes, it does seem to me likely that there are cofactors, however it also seems to me that in the terms we normally use for disease progression, XMRV is more likely than not "the" cause, or the "sole" cause. If a person were poisoned by an overdose of radiation, we would not emphasise the fact that their symptoms were not solely caused by the radiation, but were also "caused" by the lack of genetic factors that might have protected them better. Such factors will always apply to any pathology, but that doesn't change the fact that in this example, the radiation was the "cause". (It's not a great analogy but I hope you get the point.)

At this stage we just can't assume very much. To achieve rates of 80%+, XMRV seems to be fundamentally significant, but beyond that, the detail remains to be uncovered. There may or may not be cofactors; there will definitely be other factors that are relevant but whether those will constitute a "cause" is another matter.

The most significant question for the general population regards the 3-8% rate in the control groups. If XMRV has been around for 100,000 years, then that does imply that 90% of people with XMRV don't get ME/CFS - they might all be on their way to prostate cancer, MS, alzheimer's etc though. On the other hand, if the XMRV connection to 2 strains of lab mice is the result of a laboratory origin to XMRV, then we are looking at a new epidemic within the last 100 years. If that is the case, then the 4% rate would represent the "next wave" of the pandemic (those people or their descendants may be on their way to neuro-immune disease), and would suggest that rates of ME/CFS will rise in the future from 0.7% to 4%. That would be a consistent epidemiological picture in the 'modern epidemic' scenario.

The idea that there are cofactors with XMRV that determine ME/CFS progression is not a problem. But the people who try to emphasise that XMRV may be a "coinfection" or "passenger" are rather more problematic. Logically, their position is consistent in that it is a theoretical possibility, but the details of retroviral activity and of XMRV specifically mean that this would be an extraordinary coincidence if so. The people who are arguing strongly about "passengers" and "coinfections" are mostly doing so based on their existing assumptions and interests about ME/CFS.

Bear in mind that the psych lobby want to proceed from the assumption that ME/CFS is a primarily psychological condition, and to argue that immune vulnerabilities can be a consequence of personality traits and negative ways of thinking, and to therefore argue that any infections, viruses, or immune vulnerabilities are ultimately a consequence of psychological factors. In that context, with the psychological model being the predominant model for many professionals, the "coinfection" assumption will inevitably be the first argument that will occur, and the one that many people want to be the case.

But that just explains why "coinfection" and "passenger viruses" have received so much more attention than logic deserves; at the moment the most that can reasonably said is that those ideas are still "theoretical possibilities", albeit rather implausble ones.

Sorry Fejal, but about 2 million out of 300 million, is about 1 million out of 150 million, is less than 1 out 100, is less than 1%. The figure should be 0.7%. The one I've generally seen quoted previously is 0.35% to 0.7%.

Broader approaches to ME/CFS, including creating new definitions that include anybody who feels "tired all the time", can take the figure up to about 10% of the population who often feel tired, but this "fatigue" association with ME is really just the consequence of the creation of the "slave name" of "chronic fatigue syndrome". If it were called "chronic fatigue and immune dysfunction syndrome" the figure wouldn't get up above 1% quite so easily...

This is a rather transparent attempt by someone from the Marshall Protocol view to desperately hold onto the "validity" of their approach (something never proven in the first place) in the face of the emerging likelihood that much of what is making people ill could be viral, i.e. not treated by their protocol at all. What if everything built up in that edifice of tale-spinning turns out to be just plain wrong? Just like their arguments about Vitamin D?

Not only is the math operating on an erroneous assumption (just the slip of a decimal...), but nothing in the statistic to begin with, even the erroneous one, proves anything about L-form bacteria! From erroneous statistic based on over-generalization (as Mark pointed out), to a leap about co-factors as real cause, to an even greater leap that it must be "L-form, cell wall deficient bacteria." Really, nothing logical about it.

There will be a lot of folks who have invested years of time in singular approaches, or in all sorts of fallacious theories about cures for what is a hodge-podge of disease, or have been recruited by the lure of feeling important if they are members of an egoist's self-proclaimed heroism, who are having to deal with having invested time and even careers that may disappear in these light of retroviral discoveries. Beware their smug posts that "logically" attempt to bolster against the onslaught of new information.

The reality is that we don't yet know whether co-factors, predisposing conditions, or other factors are involved for some, for a few, for all, or how this will shake out. But we finally have something more than someone's private theory and anecdotal report to work on. Thank goodness!

There will be a lot of folks who have invested years of time in singular approaches, or in all sorts of fallacious theories about cures for what is a hodge-podge of disease, or have been recruited by the lure of feeling important if they are members of an egoist's self-proclaimed heroism, who are having to deal with having invested time and even careers that may disappear in these light of retroviral discoveries. Beware their smug posts that "logically" attempt to bolster against the onslaught of new information.

The reality is that we don't yet know whether co-factors, predisposing conditions, or other factors are involved for some, for a few, for all, or how this will shake out. But we finally have something more than someone's private theory and anecdotal report to work on. Thank goodness!

This is a rather transparent attempt by someone from the Marshall Protocol view to desperately hold onto the "validity" of their approach (something never proven in the first place) in the face of the emerging likelihood that much of what is making people ill could be viral, i.e. not treated by their protocol at all. What if everything built up in that edifice of tale-spinning turns out to be just plain wrong? Just like their arguments about Vitamin D?

Not only is the math operating on an erroneous assumption (just the slip of a decimal...), but nothing in the statistic to begin with, even the erroneous one, proves anything about L-form bacteria! From erroneous statistic based on over-generalization (as Mark pointed out), to a leap about co-factors as real cause, to an even greater leap that it must be "L-form, cell wall deficient bacteria." Really, nothing logical about it.

There will be a lot of folks who have invested years of time in singular approaches, or in all sorts of fallacious theories about cures for what is a hodge-podge of disease, or have been recruited by the lure of feeling important if they are members of an egoist's self-proclaimed heroism, who are having to deal with having invested time and even careers that may disappear in these light of retroviral discoveries. Beware their smug posts that "logically" attempt to bolster against the onslaught of new information.

The reality is that we don't yet know whether co-factors, predisposing conditions, or other factors are involved for some, for a few, for all, or how this will shake out. But we finally have something more than someone's private theory and anecdotal report to work on. Thank goodness!

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Bingo!
Based on Fejal's post history it's obvious he/she has some sort of interest in spreading erroneous assumptions of a totally non-proven theory. It's really a shame people or trying to make a buck out of sick people.

I think that this thread should be erased as long as it's starting message says that 7% of the American population have CFS - especially when it then goes to saying that this number is because 2.2 million Americans have CFS, and there are 307 million Americans - and as people said, that would mean that 0.7% of the American population have CFS. So that is misleading, and because this opinion is based upon that wrong number (if I understand the authour's meaning corrrectly), it is even more misleading.

That statistic is from CFS data on the web not blood testing. So your comment that the lab testing isnt specific enough doesnt apply. I do agree with you that XMRV is a trigger and that there are cofactors.

Jimk,

Im not from the Marshall Protocol. I am a patient using a modified form of it. The only thing that explains the waxing and waning of herxheimer reactions is immunopathology from L-form bacteria. I am aware that Marshall Protocol has serious flaws and I dont recommend it by itself.

>But we finally have something more than someone's private theory and anecdotal report to work on. Thank goodness!

No you dont. Because XMRV is just a trigger you are on a wild goose chase. The low viral copy number indicates that after the initial infection it isnt a problem. Wait until the antiviral drug studies come out and you get no cure. You'll spin your wheels for 10 years and end up exactly where you are now.

If the problem were L-form bacteria (which i absolutely don't believe), then:

- Where are the studies linking these bacteria to CFS?

- Is it possible to eliminate those bacteria? If so, that should lead to recovery, so where are the recovered patients? I'm not talking about a couple of cases that are not even seriously documented, there would have to be at least tens of thousands, i guess.

It might well be that XMRV is not the sole cause, but my guess is that XMRV is a sine-qua-non. Even in prostate cancer they speculate XMRV might be causal and there the prevalence in cases is much lower than in the positive CFS studies.

If the problem were L-form bacteria (which i absolutely don't believe), then:

-Where are the studies linking these bacteria to CFS?

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Lack of evidence is not evidence of lack. Where are the studies disproving it? They don't exist. What other explanations are there for a reason olmesartan elevates body temperature in CFS patients but not in normal people? None. Why do CFS patients get low grade fevers when vitamin D deprived and on olmesartan and bacteriostatics (but not without the bacteriostatics). None. Now that we know there are cofactors perhaps its time to start biopsying lymph node cells and look.

- Is it possible to eliminate those bacteria? If so, that should lead to recovery, so where are the recovered patients? I'm not talking about a couple of cases that are not even seriously documented, there would have to be at least tens of thousands, i guess.

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If course it is. They are bacteria, they have weaknesses. They need a suppressed immune system to function. They are vulnerable to bacteriostatics and their effects can be checked with olmesartan, supplements and temporary lifestyle modification. As long as XMRV doesn't chronically suppress the immune system they can be eradicated and a cure effected. XMRV isn't magic. Its immune suppression is dose dependent on the number of copies in the body. If the number of copies is low because the immune system is working then it isn't a health concern (late infection). This is no different than most viral infections. On the other hand, during the initial stage before the immune system has had time to create antibodies then the copy number is high and the system is very inhibited. Normally this clears but if L-form cofactor bacteria are around they take advantage, dysregulate vitamin D, caspase3, NF-kB and PI3 pathways for immune response effecting permanent suppression and you have CFS.

I don't understand why this is under the XMRV thread, when it is an attempt to gain attention again for the bacterial theory? Fejal has already been vocal on promoting the Marshall theory has a thread on this topic - and these should be merged with that or removed to another area.

Because XMRV is popular it means that anyone who wants attention for what their pet theory can start a topic here ostensibly on XMRV but really to promote their own ideas on entirely different things that simply don't gain the exposure that they want when the thread is not in the XMRV section.

It means that those of us who follow the XMRV section have it hijacked to try and gain exposure for theories not related at all with XMRV.

Here's his last attempt. Note no one replied in the end and he was forced to start a new topic to gain attention.

Lack of evidence is not evidence of lack. Where are the studies disproving it? They don't exist.

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That's true. But nevertheless, i would expect someone to sooner or later have made a study on this. EBV and many other agents have been studied in CFS, so why not those bacteria? Or have they and the result was not really impressive?

What other explanations are there for a reason olmesartan elevates body temperature in CFS patients but not in normal people? None. Why do CFS patients get low grade fevers when vitamin D deprived and on olmesartan and bacteriostatics (but not without the bacteriostatics). None. Now that we know there are cofactors perhaps its time to start biopsying lymph node cells and look.

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I don't know, i can't explain medical phenomena, i don't have any knowledge about these things. Sure, it would be interesting to look for those bacteria, as for any agent that might be a cofactor, so if you know of any study let me know. But i don't think they play a role in many cases, because bacteria can be fought pretty easily compared to viruses, as far as i know, and so many people have been on antibiotics that i feel like there would have to be more success-stories.

But i don't think they play a role in many cases, because bacteria can be fought pretty easily compared to viruses, as far as i know, and so many people have been on antibiotics that i feel like there would have to be more success-stories.

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A mind is like a parachute, it only functions well when it is open. The BALI Protocol is new. Look how long it took to cure polio.

should be moved as it really seems to be trying to start a discussion on a bacterial role in CFS.

Also there is no way 7% of the population has CFS. It is .7 if that. The CDC estimate of 1-4 million is using a faulty criteria and a short phone survey to identify people.

Leonard Jason has done the only prevalence surveys that I would trust and I believe he was at like 800,000-1 million. If there is around 300,000,000 people in the US then probably around .3-.33 have CCC cfs in this country.

To me this sounds about right. If you throw in Fibro, GWI and LTL the number would grow and that is worth considering especially if these folks are testing positive for MLV's.

Of course just because controls anf other NIEDS are positive for Mlv's does not mean they do not cause CFS. One virus can present differently in different individuals due to genetic variations of the host.

Some people with HIV walk around perfectly healthy for years while others get sick quite quickly so stating XMRV is in a certain amount of healthy controls therefor it could not cause CFS is not proving anything.

I am confident the WPI and the NCI will get to the bottom of the pathology of the virus before anyone else as they are way ahead of the Bell curve on this one.